Complete and revised notes from lectures original lecture notes that have been made more concise and descriptive, according to the learning objectives described for exams.
OBJECTIVES:
1. Epidemiology of cardiovascular disease
2. Pathology of atherosclerosis
3. Major risk factors
4. Interaction between risk factors + arterial wall
5. Therapies + strategies for prevention
EPIDEMIOLOGY:
- 30% of deaths in UK are cardiovascular deaths
o 70,000
- 70% of those deaths are from myocardial infarction
- Underlying cause of myocardial infarction is usually atherosclerosis
- Twice as many women die from myocardial infarction as they do from breast cancer
PATHOLOGY OF ATHEROSCLEROSIS:
- Build-up of cholesterols in the subendothelial space forms atherosclerotic plaques
- LDL cholesterols in bloodstream are absorbed by the endothelial tissue in the vessel
wall
- Oxidants in the vascular tissue in vessel wall oxidise the LDL cholesterols
- Cells respond to oxidised LDL cholesterols by increasing monocyte adhesion, foam
cell formation, cytotoxicity + vascular dysfunction
- Oxidised LDL cholesterols + responses to oxidised LDL cholesterols atherosclerotic
lesions/plaques
- Presence of plaques reduces lumen size
o Increases blood pressure
- If/when plaques rupture formation of thrombus
- Thrombus blocks blood + oxygen flow to and through the heart myocardial
necrosis
- Myocardial necrosis myocardial infarction/ischaemia heart attack death
- Early plaques (atheroma) can become stabilised plaques
o Thick fibrous cap between the small atheroma and lumen
- Can become vulnerable plaques
o Thin fibrous cap between the large atheroma and lumen
o Contains many inflammatory cells
- Ruptured plaques leak cholesterol + pro-inflammatory cytokines/neutrophils into the
vessel
o Cytokines are produced by immune cells, endothelial cells, adipocytes +
epithelial cells
- Platelets in the blood identify the collagen in the subendothelial tissue + aggregate
thrombus
- Ruptured + non-ruptured plaques are both bad because lumen is still tightened
- Presence of reactive oxidative stress (ROS) leads to pro-oxidant release
- Redox imbalances lead to molecular inflammation that causes physical + pathological
aging
Maternal Diet
Respiratory Aging
Diabetes and Aging
Brain Aging
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